Vitamin D intakes have not been assessed in national surveys and only rarely in research investigations involving smaller sample sizes. The few studies that have estimated vitamin D intakes typically find them to be below recommended amounts, especially among the elderly and, more recently, among adults. In the US, at least, most experts think that both intakes are too low and exposures of skin to sunlight are inadequate.
The few sources of vitamin D consumed in the diets of North Americans are fortified milks, fortified ready-to-eat breakfast cereals, and fish. For infants and young children who develop rickets, it has been established that they consume little milk and fish, but some cereals. No supplements containing calcium and vitamin D are ingested. For adults and the elderly, similar low consumption patterns of vitamin D-rich foods exist. Therefore, evidence strongly supports low intake of vitamin D as a major determinant of rickets and osteomalacia.
The other major determinant is poor skin exposure to sunlight, mainly to UV-B that is responsible for the conversion of 7-dehydrocholesterol to 25(OH)D3 in the dermis layer of the skin. In the US, inadequate exposure has become a major contributor over the last few decades because of concerns about skin cancer and because of increased indoor activities, including television and computers. (This poor dietary consumption and poor skin production of vitamin D seems to be paralleling the increase in overweight.) Because it is even more difficult to assess skin exposure for vitamin D synthesis, it has been extremely difficult to estimate with accuracy the additional need for dietary vitamin D. Seasonal variations yield wide swings or oscillations in skin production, depending on the position of the sun. For example, in the northern hemisphere, the highest skin production rates occur in the late spring, summer, and early autumn months (May to October), whereas in the southern hemisphere, November to April are the months of the highest
7-dehydrocholesterol ♦ D3
Jptestin Vitamin D
Hypocalcemia Hypophosphatemia PTH
> .TS intestine
Vitamin D2 or D3
No vitamin D in diet No sunlight
Liver disease Drug effects
Figure 1 Causes of vitamin D deficiency. PTH, parathyroid hormone.
Nephrectomy Renal disease Hypo-PTH Genetic defect in 1-hydroxylase
Genetic defects in receptor: Poor hormone binding Unstable receptor vitamin D production. Living near the equator extends these periods of optimal production. It is the winter months when low or even zero skin production occurs that are most problematic for the development of rickets or osteomalcia and, in the elderly, osteoporosis.
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